Information is not intended to diagnose treat or cure any condition. Please see a qualified healthcare practitioner for information and assessment if you suspect you may be suffering from PCOS.
Polycystic ovarian
syndrome is a hormone disorder affecting 5-10% of childbearing women and the
most significant cause of infertility amongst women of all nationalities. Its
classification as a syndrome means that there is a systemic nature and a
constellation of signs and symptoms that result from disordered endocrine
function. This means no two individuals with ovaries will experience it the
same. Symptoms vary greatly from weight gain, acne, excessive hair growth,
multiple ovarian cysts, and male pattern hair-loss. More advanced cases may
also result in blood sugar dysregulation (hyperinsulinemia), elevated fats in
the blood (triglycerides), and constipation and visible masses. Gone are the
days when PCOS could be ruled in or out with an Ultrasound showing cysts.
Instead diagnosis has become significantly more complicated. Currently in the
US, the diagnostic criteria include
at least two of the following: 1) light or no menses which may result in
infertility or multiple miscarriages, 2) clinical or biochemical signs of
hyperandrogenism (including excess coarse hair growth, male pattern baldness,
and/or acne), 3) polycystic ovaries.
While there is no definitive test, we can combine the clinical
picture with our understanding of an individual’s risk. The first major risk
factor is genetics; there is a strong (up to 50%) risk of developing PCOS with
a first-degree association with a family member who also has PCOS. A number of
genes have been linked to PCOS though there is no consensus yet on which
mutations will cause result in the hormonal dysregulation seen in
PCOS. Obesity is another risk factor for PCOS, while, weight gain is a common
symptom of PCOS. Stress can also increase the risk for atypical PCOS,
since it can disturb the hypothalamic pituitary axis (HPA) which lowers most
sex hormones. Further, insulin resistance means there is more insulin in the
bloodstream which promotes androgen production, which then exacerbates insulin
resistance. This upsets the delicate hormone balance in the body, having
widespread systemic effects.
Two theories exist to
explain the excess androgens (testosterone and DHEA) present in individuals
with ovaries:
1. The first theory is
that the rhythm of reproductive hormones from the hypothalamus and anterior
pituitary are disturbed. Meaning it is a central dysfunction. Normally the
little gland in our brain known as the hypothalamus releases gonadotropin
releasing hormone (GnRH) which can then travel to the neighbouring pituitary
gland resulting in release of luteinizing hormone (LH) and follicle stimulating
hormone (FSH) (LH:FSH ratio is increased). With these levels increased follicles
(or eggs) are not able to properly mature and then cannot be released (anovulation),
and abnormal or no menstruation. Without ovulation of follicles, estrogen
levels rise because they are unopposed. This promotes androgen production in
the ovaries as well as in fat tissue where excess estrogen is converted to
testosterone.
2. The second theory,
that may simultaneously happen, is that women with PCOS seem to have high
levels of insulin in their blood, indicating an insulin resistance. These
high insulin levels contribute to this hormone dysregulation independently to
the HPA axis. Insulin can stimulate the ovaries and adrenal glands to increase
production of androgens and can also have an effect on the
hypothalamus. Insulin also reduces the amount of sex hormone binding
globulin (SHBG,) this means more androgens are floating around and available
for longer than normal. This hormone dysregulation has a significant impact on
fertility since women have difficulty ovulating, which can lead to the
development of ovarian cysts, hence the name.
In both cases individuals may experience very significant psychological
effects of PCOS, including depression, anxiety, and body dysmorphia. This can
have a profound impact on well-being particularly when dealing with
infertility. The overall goal of treatment is to rebalance hormones by
increasing the excretion of excess estrogen, resetting the complex feedback
systems that control it, promoting ovulation, and rebalancing blood sugars.
Lifestyle considerations
include fat loss through high intensity interval exercise, particularly if
there is significant abdominal fat present. Other steps that can help are the
removal of toxic endocrine disruptors found in foods and personal care products
and increasing elimination pathways, with good bacterial environments and
fibre. Further, ensuring the timing of meals supports proper blood sugar
management and consuming low glycemic index foods, avoiding saturated and
trans-fats, and simple sugars.
Supplementation may also
be indicated for certain individuals with deficiencies or genetic abnormalities.
Inositol is a member of the B vitamin family
comes in two forms the myo-inositol and d-chiro- inositol. It acts like a
secondary messenger, communicating with cells in the brain and for resetting
the “hormonal thermostats.” A combination of the two forms was shown to
significantly improve insulin sensitivity by cells, thus preventing blood
glucose dysregulation. This also had an impact on a regulating number of sex
hormone levels. Further, oocyte and egg quality improved leading to
improved fertility in women suffering from PCOS. This treatment option is
particularly helpful for induvial who have significant mood disruption as it is
also known to be calming while still addressing underlying cellular causes and
insulin regulation.
Folate has also been seen to be beneficial by providing
antioxidant support from excess homocysteine. Folate also supports healthy
brain, cardiovascular and genetic functioning. It is very important to ensure
that individuals are able to convert and use the folate from supplements. A
genetic anomaly known as the MTHFR mutation prevents folic acid commonly found
in supplements from being converted into its active form and participating in
the neutralisation of a toxic product called homocysteine. So by providing the
calcium-5- methyltetrahydrofolate form of folate we reduce the metabolic burden
on individuals while also considering the high incidence of this mutation. Other
treatments to promote healthy cellular functioning and hormone regulation
include: vitamin D, and chromium picolinate, and alpha lipoic acid,
supplementation to improve insulin resistance, and N-acetyl cysteine.
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